We studied dynamic changes in the total number of cardiomyocytes and the character of structural lesions in the myocardium in rats with modeled anthracycline-induced cardiomyopathy provoked by a single injection of doxorubicin in a dose of 10 mg/kg alone or in combination with subsequent adrenergic stimulation. The injections of epinephrine during the development of anthracycline-induced cardiomyopathy resulted in more pronounced loss of body weight, stronger decrement of the heart weight, and more severe decrease of the cardiomyocyte count in comparison with the corresponding changes induced by doxorubicin alone. The basic lesions of cardiomyocytes in anthracycline-induced cardiomyopathy are the lytic alterations and subsegmental contractures; in contrast, combined use of doxorubicin and epinephrine provoked degree II and III contractures. The revealed necrobiotic changes of cardiomyocytes resulted in their death and pronounced decrease of their number at the initial terms of the study. Hypertrophy observed at later terms of the experiments in parallel with partial recovery of cardiomyocyte number reflected the development of regenerative and adaptivecompensatory processes induced by massive death and elimination of the parenchymatous cells (up to 36-37% of population).
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http://dx.doi.org/10.1007/s10517-019-04419-x | DOI Listing |
J Card Fail
January 2025
Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, MA, USA.
Background: Data on left ventricular ejection fraction (LVEF) recovery in patients with anthracycline-induced cardiomyopathy (AIC) are limited.
Objectives: To evaluate LVEF recovery rate, its predictors and association with cardiovascular outcomes in a contemporary and diverse AIC cohort.
Methods: This retrospective study analyzed patients diagnosed with AIC from 2010-2023 at two U.
J Cardiovasc Pharmacol Ther
January 2025
Department of Clinical Pharmacy, University of Michigan College of Pharmacy, Ann Arbor, MI, USA.
Background: Neurohormonal blocking drugs, like beta-blockers, angiotensin-converting enzyme inhibitors (ACEIs), and angiotensin receptor blockers (ARBs), are recommended for treating anthracycline-induced left ventricular dysfunction (AILVD). However, there is limited evidence supporting their benefit. Therefore, this study evaluated associations of neurohormonal blockers and other clinical factors with recovery of left ventricular ejection fraction (LVEF) in patients with AILVD.
View Article and Find Full Text PDFCurr Cardiol Rep
December 2024
Division of Cardiology, Department of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Purpose Of Review: In this review we describe the role of inflammation in chemotherapy-induced cardiotoxicity with a particular focus on anthracycline-induced cardiomyopathy (AIC). First, we discuss inflammation associated with anthracyclines at a cellular level. Next, we discuss the clinical implications of these inflammatory mechanisms for early detection and cardioprotective strategies in patients undergoing anthracycline treatment.
View Article and Find Full Text PDFBMC Cardiovasc Disord
September 2024
Department of Cardiology, Niigata City General Hospital, 463-7, Shumoku, Chuo-ku, Niigata, 950-1197, Japan.
Cureus
August 2024
Internal Medicine, Mayo Clinic, Rochester, USA.
Advances in the field of oncology have led to the advent of doxorubicin (DOX), an anthracycline chemotherapeutic agent, through which cancer survival rates have remarkably improved. There has, however, been a rise in adverse effects from the use of DOX, most notably cardiotoxicity. DOX-induced cardiotoxicity is thought to arise through the generation of reactive oxygen species (ROS), causing mitochondrial dysfunction in the cardiomyocytes.
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